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Redox homeostasis genes modulate response to APR-246 in a p53-dependent and p53-independent manner Previous studies have characterized APR-246 as a modulator of redox homeostasis and inducer of ROS through depletion of key antioxidants, resulting in both p53-dependent and -independent cell death pathways such as ferroptosis [26,27,28,29]
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A rare spontaneous finding
Pretreatment with thymulin reduced, in a dosedependant manner, the ETinduced hyperalgesia, and exerted differential effects on the upregulated levels of cytokines in different areas of the brain, suggesting a neuroprotective role for thymulin in the central nervous system (CNS)
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